Endometriosis is a gynecologic disorder which can be deleterious to fecundity as well as general well-being. Nearly 10 percent of reproductive-aged women suffer from dysmenorrhea, menstrual irregularities, chronic pelvic and back pain, and infertility associated with extrauterine endometriosis implants. The clinical disorder is hormonally-sensitive, but the precise mechanisms by which endometriosis is initiated or exacerbated by ovarian steroid hormones have not been defined. The classical work of Markee (1940) indicated that these steroids play an important role in the vascularization of normal endometrium. Indeed, neovascularization of peritoneal implants appears to be a critical step in the pathophysiology of this disorder. Vascular Endothelial Growth Factor (VEGF), interleukin-6 and prostaglandin E2 have known angiogenic potentials and may thus play an important role in the development, growth and progression of endometriosis implants. Our laboratory has demonstrated that normal endometrial VEGF mRNA and protein are regulated by estrogen and progestin. The goals of this study are to evaluate the importance of these angiogenic factors in the establishment of extopic endometrial implants and to define the regulation of VEGF production in isolated endometrial and endometriosis cells.